Treatment of esophageal disorders caused by medications, caustic ingestion, foreign bodies and trauma

SECTION THREE MANAGEMENT OF ESOPHAGEAL DISORDERS

16

CHAPTER SIXTEEN

Treatment of esophageal disorders caused by medications, caustic ingestion, foreign bodies and trauma Umesh Choudhry and Henry Worth Boyce

ESOPHAGEAL INJURY CAUSED BY MEDICATIONS Introduction Esophageal injury due to ‘pills’ was first reported by Pemberton in 1970.1 Since then, nearly 100 drugs have been reported to incite injury to the esophageal mucosa (Table 16.1).2–4 Drugs that have been most reported to cause esophageal injury include potassium chloride (especially the slow release, wax matrix form), tetracycline, doxycycline, quinidine gluconate, ferrous sulfate, nonsteroidal antiinflammatory drugs (NSAIDs) and more recently, alendronate, zidovudine, rifampin and lansoprazole.5,6 Emepronium, a common cause of drug-induced esophageal damage (DIED) in parts of Europe, is not available in the United States. Esophageal injury caused by medications can be classified into two categories. The first type of injury is an acute, superficial injury of a short duration. Spontaneous healing after discontinuation of the offending agent is the rule. The second type of injury is characterized by deep, intramural inflammation and ulceration, which heals by stricture formation. The late sequelae of this latter type of injury are difficult to treat and place considerable limitations on the patient’s lifestyle.

Pathogenesis The pathogenesis of DIED is best understood by examining the properties of the drug formulation, the shape and form in which the drug is swallowed, the habitus and characteristics of the patient who ingests the medication, and the functional status/anatomy of the esophagus. The most critical factor in the development of DIED is the contact time of the injurious drug with the esophageal mucosa.

Agent factors The drug delivery vehicle, whether pill or capsule, is important because the latter can adhere to the esophageal wall and dissolve slowly, thereby increasing the contact time of the drug with the mucosa. The hygroscopic property of gelatin capsules and their sticky surface allows them to adhere to the mucosa. Thus, doxycycline tablets were found to be less ulcerogenic than the capsule form of the same medication.7 Large tablets, especially those larger than 13 mm in size are more likely to get lodged at a site of

‘physiological narrowing’ in the esophagus, such as at the aortic arch level.8,9 Oval-shaped, film-coated tablets traverse the esophagus easier than round, uncoated tablets.9 The chemical nature of the drug is another important factor. Some medications such as doxycycline, ferrous sulfate, ascorbic acid, or aspirin cause esophageal damage due to their acidic nature.7,10–12 Aspirin may also increase the permeability of the mucosal barrier, allowing H+ ions into the cells.13 Although other medications, such as quinidine gluconate and potassium chloride, have a neutral pH, they incite damage by the hyperosmolar solution produced by dissolution of the drug.14 Direct thermal injury may be produced by dissolving of the agent/medication, as occurred in the case of Clinitest (copper sulfate) tablets. These tablets, now off the market, were used for detecting urine glucose in diabetics and were ingested accidentally or deliberately.15

Host factors DIED is more common in the elderly, debilitated population because they take more medications and are typically in a recumbent position for longer periods of time. These patients also secrete a reduced amount of saliva. In healthy adults, more than one ounce (30 cc) of water is required to swallow and reliably pass a 13 mm tablet promptly into the stomach.16 Therefore, when medications are ingested without or with an insufficient amount of liquid, the chance they will persist in the esophagus is increased.17–19 Even when the esophageal lumen is normal, elderly patients or those confined to a bed are at a higher risk for medications adhering to their esophageal mucosa, due to protracted recumbency.9,18 In addition, poor memory or visual impairment may interfere with their ability to read and comprehend the instructions on the package.

Esophageal factors In addition to the natural propensity for medicines to traverse the sites of anatomical narrowing in the esophagus (cervical esophagus, aortic arch level, and lower esophageal sphincter), underlying esophageal pathology, such as abnormal esophageal motility, a pre-existing stricture, or cardiomegaly (left atrial esophageal compression), may compound the risk of injury due to medications. Hiatal hernias, a very common condition in Western populations, have been shown to reduce the transit of ingested pills.20 Similarly, a Schatzki ring less than 13 mm in diameter may contribute to the delayed transit of tablets.11

Treatment of Esophageal Disorders caused by Medications, Caustic Ingestion, Foreign Bodies and Trauma

242 Table 16.1 Various drugs causing esophageal disease Class of drug Major offenders Potassium chloride (delayed release)

achalasia.2,7 Prevention and treatment strategies are summarized in Table 16.2.

Agents

Slow K & other KCI formulations

Antiarrythmics

Quinidine gluconate, quinidine sulfate

Antiosteoclastic

Alendronate

Diuretic

Furosemide

Antibiotics

Doxycycline, other tetracyclines, penicillin, clindamycin

Antiinflammatory drugs

Aspirin, indomethacin, piroxicam ibuprofen

Other offenders Antiviral agents

Zidovudine

Vitamins

Ascorbic acid, multivitamins

Iron preparations

Ferrous sulfate/succinate

Miscellaneous

Mexiletine, captopril, theophylline, warfarin,

Agents not available in the United States

Emepronium bromide, pinaverium

Prevention of drug-induced esophageal damage Esophageal injury due to medications is entirely preventable. The lack of knowledge of physicians, pharmacists, and patients is the biggest hurdle in preventing this injury. Dissemination of information regarding the injurious potential of various medications is therefore essential. Pharmaceutical companies have the primary responsibility of informing and educating the medical community, using unambiguous language, about the injurious potential of drugs. Package inserts of such medications should contain explicit instructions regarding their use. All physicians and nursing personnel should similarly educate patients, hospital/nursing, home personnel, and caregivers at all levels. Although potassium chloride (Slow-K) was identified as being injurious to the esophagus over 30 years ago, many internists and cardiologists remain unaware of this potential problem with potassium chloride.1 Patients should be warned prior to initiation of therapy with these high-risk agents. Periodically during therapy, a careful history for odynophagia, retrosternal pain, and dysphagia should be obtained. Special attention should be given to patients who are taking multiple medications. Medications that reduce salivary secretions or esophageal peristalsis (e.g., antihistamines, anticholinergics) are likely to increase the contact time of injurious medications with esophageal mucosa, thereby worsening the damage. All patients should be advised to take medications in an upright posture, take at least 2–3 oz water with each tablet, and to remain upright for at least 15 minutes after ingestion.21 When medications are prescribed to be taken at bedtime, patients should be informed that ‘at bedtime’ does not mean at the time of recumbency, but rather 15 minutes or longer before assuming a recumbent position. Liquid preparations should be used for bedridden patients and patients with preexisting esophageal lesions such as strictures, diverticula, and

Diagnosis and treatment of drug-induced esophageal damage in the acute phase As previously outlined, an accurate history leads to an early diagnosis in most cases. Patients with DIED present most often with a burning retrosternal pain (60–70%).4 Odynophagia is the second most common symptom (50–74%); however, dysphagia is relatively infrequent and usually is reported when there is a significant luminal compromise during the later stages of injury.22 Pain, odynophagia, and dysphagia can develop within hours to 10 days after the initiation of the medication. The first and foremost step in this phase of injury is to identify the offending agent and discontinue its use. If a pill is found adherent to the mucosa or impacted in the esophageal lumen on a barium swallow, early endoscopy may be required for its removal. Symptomatic treatment using antacids, topical xylocaine gel or a combination and oral analgesics are useful in alleviating pain. These combinations may be named variously in different hospitals as ‘GI cocktail,’ ‘Kessler’s solution’ or ‘magic mouthwash.’ They are usually short acting and must be administered frequently. Sucralfate, H2-blockers, and proton pump inhibitors have also been used to promote the healing of acid reflux-related ulceration/erosion of the esophagus, although their efficacy in treatment of DIED has not been established.2,3,23 No further diagnostic evaluation for acute symptoms is recommended in younger patients without immune deficiency states.3,8 If symptoms persist or worsen despite the above measures, the patient should undergo an esophagogastroduodenoscopy (EGD). A double-contrast barium esophagogram may be helpful as an initial study, but EGD has the advantage of revealing more mucosal detail. It also provides a more accurate assessment of the degree of injury and gives an opportunity for biopsy. Impacted tablets/capsules, if encountered, can also be removed at the time of the procedure. In 99% of cases, mucosal abnormalities are found on EGD and commonly include a single, shallow, discrete ulcer with exudate at the level of the aortic arch or circumferential mucosal ulceration or nodularity of the mid esophagus with an adherent clot.4,24

Table 16.2 DIED: prevention and treatment strategies Prevention Physician/pharmacist education Patient education: upright posture and 100 cc water Modification of pill size/shape Substitution of pills by elixir or orally dissolving formulations Avoid concurrent use of offending agents Treatment during acute phase Cessation of offending agent Symptomatic treatment: topical and oral analgesics, antacids, sucralfate Treatment after stricture formation Esophageal dilation Intralesional triamcinolone injection: questionable benefit Surgery: almost never required

243

Management of delayed sequelae of drug-induced esophageal damage When medications cause a deep ulceration of the esophageal wall, the healing phase is prolonged and slow. Persistent symptoms often indicate complications such as stricture formation, bleeding, or perforation.19 The medications usually implicated in this type of injury include a delayed-release wax-matrix form of potassium chloride (Slow-K), quinidine gluconate (Quinaglute), and indomethacin. A recent addition to this list is the daily dosing version of bisphosphonate: alendronate (Fosamax 10 mg).27,29,30 When patients present with continued symptoms and a history of ingestion of one of the above mentioned ‘serious offenders,’ it is important to proceed with an early endoscopy due to the serious transmural injury caused by these agents.31,32 If active ulceration is identified by barium study or EGD, acid suppression in the form of H2-blockers or proton pump inhibitors is indicated in patients with gastroesophageal reflux. Esophageal dilation is postponed until inflammation/ulceration is completely healed. Esophageal dilation in the presence of ulceration is often ineffective and may be associated with complications.33 Once inflammation is resolved and stricture formation is confirmed, the stricture should be dilated early and frequently, to prevent contraction of the cicatrix.19,26 Unfortunately, patients may be seen by gastroenterologists months to years after the initiation of these medications because some drugs such as potassium chloride and quinidine gluconate may not cause odynophagia or retrosternal pain. In other cases, repeated complaints of dysphagia are often ignored until a tight, fibrotic stricture develops, at which point esophageal dilation becomes very difficult. These patients require multiple sessions of esophageal dilation performed at 1–2 week intervals, usually over several months.26 Almost all patients show gratifying results and have nearly complete resolution of symptoms after adequate esophageal luminal patency has been restored. Since multiple sessions of esophageal dilation are anticipated, the pathophysiology of the condition and treatment plan should be discussed in detail with the patient. The patient may be given appointments for several sessions of dilation in advance to assure proper treatment intervals. The median number of dilation sessions required over 6–12 months to achieve adequate lumen patency for severe quinidine gluconate-related strictures at our center is 14. Dilation over a wire guide is the preferred method for these strictures. Several investigators have described the use of intralesional injections of triamcinolone in ‘refractory’ strictures.34–39 A MEDLINE review of the use of intralesional steroids revealed several case reports, primarily in patients with corrosive strictures, one retrospective study, and one randomized prospective study (in abstract

form) of patients with reflux strictures.34–39 All report a decrease in the frequency of dilation after intralesional steroids. However, none of these reports defined ‘stricture’ relative to the degree of active inflammation present, and only one patient had a DIEDrelated stricture. Intralesional injection of steroids is simple and safe, with no serious reported adverse effects. However, it is useful only for strictures less than 1 cm in length. A 23–26-gauge endoscopic needle (sclerotherapy needle) is used to inject 40 mg/mL strength triamcinolone or a larger volume of diluted strength. Four quadrant injections of 0.5 mL each are made at the time of each dilation. The benefit shown with the use of intralesional steroids has likely been due to their antiinflammatory property. However, satisfactory results can be achieved with conventional dilation performed with a proper technique. There is currently no proof that steroid injections relieve obstructions in chronic fibrotic strictures not associated with active inflammation. We ascribe the therapeutic success to the elimination of inflammation, discontinuation of the offending agent, and wire-guided dilation under fluoroscopy. The use of intralesional steroids is not recommended as a standard therapy in patients with DIED.

Role of surgery/stents Surgery has no proven role in the treatment of DIED, except when perforation or uncontrollable bleeding occurs. All strictures can be successfully managed by wire-guided dilation. The use of selfexpanding metal or nonmetallic stents for benign esophageal strictures has been evaluated over the past few years. The experience to date suggests that this approach leads to significant complications and should be avoided in patients with significant life expectancy and who have other treatment alternatives.40,41

ESOPHAGEAL INJURY CAUSED BY CANCER CHEMOTHERAPY Introduction Cancer chemotherapy alone or in conjunction with radiation therapy often results in esophageal damage. The damage is often diffuse and similar to mucosal injury that occurs elsewhere in the body.42,43 Patients typically present with severe odynophagia and dysphagia. Intense nausea and vomiting are caused by the chemotherapeutic agents and reduce the ability of the patient to ingest oral liquids. On endoscopy, diffuse erythema with exudation is seen throughout the esophagus. Bleeding may occur and may be potentiated by thrombocytopenia or coagulopathy secondary to bone marrow suppression. Immunosuppression may also result in opportunistic esophageal infections due to Candida, herpes simplex virus, or cytomegalovirus.

Symptomatic treatment Amelioration of retrosternal pain and odynophagia is the first goal of treatment, followed by treatment to promote healing. Topical analgesics are often useful for the mucositis that nearly always accompanies esophagitis. Viscous xylocaine can provide some measure of relief, albeit short-lived, from pain and odynophagia. Due to its short duration of action, xylocaine jelly alone or in combination with antacids needs to be given at frequent intervals (every 1–2 hours, up to a maximum of 8 doses of 15 mL in

Esophageal Injury Caused by Cancer Chemotherapy

The mucosa above and below this lesion is generally normal,7,25 although on occasion, a distal esophageal ulceration maybe be found, especially in the presence of a pre-existing reflux-related injury.26,27 Pill remnants or pigmentation of the mucosa may also be seen. On histological examination, the pigmentation has been shown to be due to impregnated crystals of the offending medication, viz., ferrous sulfate or doxycycline.28 Most cases of DIED improve with cessation of the offending medication plus symptomatic therapy in the acute phase and do not require any further treatment.29 Pre-existing lesions, when identified, should be managed appropriately for complete resolution of symptoms.

Treatment of Esophageal Disorders caused by Medications, Caustic Ingestion, Foreign Bodies and Trauma

244 24 hours). Oral/parenteral pain medications may be required, in addition to topical analgesics. When used, it is best to prescribe these medications as alcohol-free suspensions since alcohol typically exacerbates pain and odynophagia. Combinations of acetaminophen and codeine or hydromorphone are useful in this situation. Cryotherapy using ice chips in the mouth has been used to prevent oral mucositis in patients receiving chemotherapy.44 Similarly, sucralfate has been studied in prevention and treatment of chemotherapy-induced stomatitis.45 It is uncertain if sucralfate has any proven effect in the treatment of chemotherapy-associated esophagitis. Because acid suppression therapy using H2-blockers or proton pump inhibitors is traditionally used for reflux esophagitis or peptic ulcer disease, these medications are often used in patients with esophagitis due to chemotherapy despite lack of any substantial evidence indicating a benefit.46 Supportive measures such as adequate nutrition and hydration by the parenteral route or a thin nasogastric tube for enteral feeding are important. It is preferable to pass the nasogastric tube under fluoroscopic guidance. Acid suppression by either an H2-blocker or a proton pump inhibitor should be given during nasogastric intubation.

ESOPHAGEAL INJURY CAUSED BY LYE/CAUSTIC SUBSTANCE INGESTION Introduction Lye-based liquid household cleaners have been commercially available in the United States since 1967. Accidental and intentional ingestion of these substances has resulted in serious morbidity during the past three decades. It is estimated that caustic ingestion and foreign body aspiration are the third most common causes of pediatric death in this country.47 Nearly 26 000 episodes of caustic substance ingestion occur in the United States every year. Nearly 17 000 of these involve children, 50% of whom are under the 4 years of age. Adults and adolescents account for 20% cases, the majority of which are suicidal gestures. The agents most often reported to be involved in these cases are shown in Table 16.3.

Table 16.3 Common household corrosives Brand name/product

Chemical name

Red Devil Drain Opener

Sodium hydroxide (96–100%)

Crystalline Drano

Sodium hydroxide (50%)

Clinitest tablets

Sodium hydroxide (50%)

Liquid Drano

Sodium hydroxide (2–10%)

Signs and symptoms of caustic injury Several large series of caustic ingestion esophageal injuries have been reported.48–50 The signs and symptoms reported include nausea, vomiting, dysphagia, refusal to drink, drooling, and stridor. None of these signs and symptoms appears to accurately predict the degree of injury. Crain and colleagues reported that the presence of two or more of the serious signs/symptoms, namely vomiting, drooling, or stridor, indicated a 50% chance of esophageal injury.50,51

Pathogenesis Vancura and colleagues, using a cat model, demonstrated that alkali at a pH of 12.5 produces esophageal ulceration.52 Liquid lye, frequently available in the form of drain cleaner, produces its injury by liquefaction necrosis and is thus able to quickly spread into the esophageal and gastric mucosa, thereby producing widespread penetrating injuries. Bacterial infection regularly occurs and potentiates the injury. Acidic caustic substances (except hydrofluoric acid), in contrast, result in coagulation necrosis and form a thick eschar, which may protect the mucosal layers from damage. By 10 days after caustic injury, granulation tissue begins to replace the necrotic tissue, and fibroblast proliferation and scar formation begin by the third week after injury. Caustic ingestion may cause serious systemic effects by causing airway edema and obstruction, resulting in hypoxia and hypercapnia. Metabolic disturbances can occur and require immediate attention. Infection usually complicates the clinical scenario in cases of esophageal perforation.

Prevention of corrosive injury In most instances, injury due to corrosive substances is preventable. Educating the public regarding proper storage of these agents away from the reach of infants and children and possibly from suicidal adolescents is required as a continuous effort. Educating prospective parents during prenatal classes when their attention level is heightened may be another strategy. Efforts from industry are needed to minimize the corrosive component of household cleaning solutions. Proper labeling and addition of colors to these agents can prevent their being mistaken for water. In addition to household cleaners, corrosive alkali is present in cylindrical and button batteries. There is thus a need for manufacturing leak-proof battery casings, as merely sucking on a battery by a child has been reported to result in esophageal burns.53 Some countries such as Norway have taken a lead in this matter and have banned the sale of alkaline corrosives as household cleaners. Ironically, acid injuries now account for a majority of cases in Finland.54

Mr. Clean liquid

Sodium carbonate

Top Job liquid

Sodium carbonate/ammonia

Phases of corrosive injury

Liquid clorox

Sodium hypochlorite (5.25%)

Three phases of corrosive injury have been described.55 A thorough understanding of these phases is important in planning a therapeutic strategy.

Lysol deodorizing cleaner

Ammonium chloride (2.7%)

Swish toilet bowl cleaner

Ammonium chloride (1.25%)

Dish water detergents

A combination of sodium hypochlorite, bicarbonate, phosphate, silicate (pH: 12.5)

Battery fluid

Sulphuric acid

Acute phase The first 72 hours after the ingestion of the corrosive substance constitute the acute phase. It is characterized by the initiation of an inflammatory response and vessel thrombosis. Invasion of the

245

Subacute phase This phase spans from 3 days to 3 weeks post corrosive ingestion. An intense inflammatory response and further vascular thrombosis occurs during this phase, resulting in sloughing of the superficial layers of mucosa and ulceration. Granulation tissue formation, fibroblast infiltration, and collagen deposition also occur and may be accompanied by significant hemorrhage. The risk of esophageal perforation is increased, especially with blind instrumentation such as nasogastric intubation during this phase.

Chronic phase Beginning at about 3 weeks post ingestion, the chronic or late phase of corrosive injury is marked by scar retraction, continued fibrosis, mucosal re-epithelialization and possible tracheoesophageal fistula formation. Stricture formation occurs in up to 30% of patients with corrosive esophageal injury, typically in patients with second and third degree injury.56 These patients have been estimated to have a greater than 1000-fold increase in the incidence of squamous cell carcinoma of the esophagus 15–20 years after corrosive ingestion,57,58 and periodic surveillance should thus be considered in this group after 15 years. The use of Lugol iodine chromoendoscopy will delineate foci of dysplasia or cancer and can enhance early diagnosis.

Treatment in the acute phase Patients who can give a reliable history of accidental ingestion, are asymptomatic, have no evidence of oropharyngeal burns, or have only a questionable history of corrosive ingestion may be observed in the emergency room or during an overnight hospital stay. In contrast, patients who show signs of acute injury, may have ingested large amounts of corrosive substances or are suicidal should be admitted to the intensive care unit for observation, further diagnostic tests, and treatment. In either situation, early endoscopy will provide an accurate assessment of the degree of injury.

Airway protection Emergency tracheostomy or endotracheal intubation is indicated in patients with stridor, hoarseness, or inability to speak. It should be borne in mind that the onset of respiratory symptoms may be delayed up to 24 hours. PA and lateral chest X-rays should be obtained initially and repeated, based on the patient’s condition, since aspiration pneumonia is a risk in these patients.

Most patients need to be kept NPO in view of the possibility of endoscopy or surgery. Patients who are able to swallow their saliva, do not have any respiratory symptoms, or in whom urgent endoscopy is not contemplated may be allowed ice chips or sips of water.

Endoscopic evaluation and management As stated above, signs and symptoms do not generally predict the severity of damage. Since treatment options depend greatly on the assessment of injury (Table 16.4), endoscopic examination should be carried out as early as possible. This strategy also minimizes the risk of perforation. Endoscopy should be done 24–48 hours post ingestion or sooner if respiratory and hemodynamic parameters are stable. More than 50% of patients with a history of caustic ingestion are found to have no evidence of esophageal injury on an early endoscopy.49,50,60,61 The extent of the endoscopic examination has also been debated. In the past, when endoscopes were rigid, a limited examination within the first 24 hours was favored to avoid perforations.62,63 Endoscopists terminated the exam at the level of the first burn site. With the availability of small-caliber flexible video endoscopes, endoscopy under direct vision is considered safe during any phase of the illness in the absence of obvious evidence of perforation.64 Some authors recommend gently guiding the instrument through areas of superficial injury and continuing examination until areas of possible full-thickness necrosis are encountered, an approach that allows complete evaluation of the upper gastrointestinal tract and has been reported to be safe.65–67 If severe full-thickness necrosis is encountered, the examination is terminated and intensive care observation continued for signs of esophageal or gastric perforation. Endoscopic management strategy is summarized in Table 16.5.

Nasogastric tube placement There have been reports in which acute corrosive injury was managed conservatively by the insertion of a nasogastric tube.68 Although no controlled data are available regarding this approach, the nasogastric tube appears to act as a stent and prevents complete occlusion of the lumen and assures access for dilation guidewire

Table 16.4 Endoscopic grades of corrosive injury 1st degree

Erythema, edema, erosions (bleeding)

2nd degree

Intense erythema, blebs, and deep erosions with exudate

3rd degree

Epithelial loss, ulceration, necrosis, exudate and eschar

Supportive treatment Appropriate management of hypotension and shock may be required in the form of intravenous fluids or pressor agents. Surgical consultation should be obtained early in cases of severe esophageal injury as emergency surgery is indicated if evidence of esophageal, gastric, or other visceral perforation is present. Signs of esophageal perforation include pneumomediastinum, subcutaneous emphysema, crepitus, dyspnea, and severe chest or abdominal pain. Care should be taken to avoid the use of emetic agents as they may precipitate additional esophageal and oropharyngeal injury and lead to perforation. The use of neutralizing agents is contraindicated as neutralization reactions lead to heat production and may further aggravate the injury.59

Table 16.5 Endoscopic management of corrosive injury General anesthesia usually not required Early endoscopy post stabilization Complete, diligent examination of the esophagus and stomach Repeat EGD after 2 weeks Initiate dilation before 3 weeks if evidence of stricture Savary dilation over guide wire under fluoroscopy is optimal technique for initial therapy

Esophageal Injury Caused by Lye/Caustic Substance Ingestion

esophageal wall by bacteria and polymorphonuclear leukocytes takes place during this phase.

Treatment of Esophageal Disorders caused by Medications, Caustic Ingestion, Foreign Bodies and Trauma

246 placement. If a nasogastric tube is used, it should be connected to low intermittent suction to avoid gastric distention. Measures to prevent acid reflux such as elevation of the head of the bed and acid suppression should also be employed during intubation. Some authors favor this approach if severe esophageal damage has been ruled out by endoscopy. In our opinion, when nasogastric intubation is considered appropriate, the concomitant use of an intravenous proton pump inhibitor is indicated. It is safer to place the nasogastric or nasoduodenal tube under fluoroscopic guidance or over a wire placed through the endoscope after evaluation has been completed. If the nasogastric tube tip is modified prior to placement by removing the blind end tip and smoothing the cut edges, guidewire insertion at the time of dilation can be done through the tube with safe post-dilation replacement of the nasogastric tube over the guidewire.

Use of corticosteroids, antibiotics, and early dilation Since 1950, the use of systemic corticosteroids has been advocated in the acute and subacute phases of injury. Spain and colleagues reported a reduction in the degree of inflammation in an animal model.69 However, Anderson and colleagues, in a prospective study, refuted this claim and reported no improvement in the steroidtreated group.60 This debate may have been rekindled by a recent study by Bautista et al., who showed dexamethasone to be superior to prednisone in preventing strictures and reducing burn severity at 3 weeks. The dexamethasone-treated group also needed fewer dilations.70 Barring this study, the prevailing belief at the present time is that steroids do not play a role in the treatment of corrosive injury.71,72 The positive effect of dexamethasone in children may also be related to the fact that children, unlike suicidal adults, are brought to the hospital very early during the postingestion period. Antibiotics alone have not been shown to be of any benefit in the treatment of corrosive injury. Their use has been limited to the prevention of septic complications in patients on intravenous corticosteroids.73 Broad-spectrum antibiotic therapy is indicated in patients with signs of esophageal or gastric perforation. Esophageal dilation carried out in the subacute phase may be associated with an increased risk of perforation.74,75 In contrast to traditional thinking, esophageal dilation using proper technique and fluoroscopic control may be safe even during the subacute phase. Early dilation and the prevention of stricture formation forms the basis of the modified Salzer technique described by Palmer.67,76 Using fluoroscopic guidance and proper technique, the patient receives a nasogastric tube within a few hours of the corrosive ingestion. Wire-guided esophageal dilation is then initiated on the third day after an endoscopic examination, with the dilator size chosen based on the age of the patient. Adult patients may be started with a 12 or 13 mm dilator (5–6 mm for a child); the dilation may be gradually progressed by 1–2 mm to reach a 15 mm diameter by the end of the first month. The dilation is discontinued if fresh blood is seen on the dilator. Dilations are carried out at least two or three times per week for several weeks in order to prevent stricture formation. Dilations predictably meet more resistance by the fourth week. The diameter of the lumen and frequency of dilation sessions should be determined by the resistance experienced on passage of each dilator. A progressively less frequent dilation schedule should be set for the next several months to years, using either wire-guided dilation or Maloney bougie dilation under fluoroscopic control to maintain lumen diameter between 15 and 18 mm. Periodic radiographic and endoscopic evaluations

should be continued as indicated for dysphagia and surveillance for the remainder of the patient’s life.

Total parenteral nutrition Maintenance of nutrition is of utmost importance in seriously ill patients. Feeding through the nasogastric tube may not be possible in patients with severe (grade 3) injury or in patients with impending perforation. These patients should receive early total parenteral nutrition (TPN) to avoid malnutrition, while allowing the gastrointestinal tract to rest and heal. DiConstanzo and colleagues reported that TPN protects the damaged mucosa.77 TPN may also be required during the perioperative period in patients who require surgery.

Surgery Esophagectomy should be performed when evidence of perforation related to the acute-phase injury is present. When endoscopic examination reveals extensive gastric necrosis, most authors recommend esophagectomy with gastrectomy and anastomosis, as either a oneor two-stage operation. Surgery is performed with the presumption that esophageal perforation is imminent in this situation. Zargar and colleagues proposed a modified classification system for corrosive injury and further subdivided second and third degree injury into grades 2a, 2b, 3a, and 3b. Patients with grade 1 (erythema and edema) and grade 2a injury (friability, hemorrhages, erosions, and superficial ulceration) did not develop any complications. Grade 2b (deep discrete or circumferential ulcers) or deeper injury was associated with complications. Patients with small and scattered areas of necrosis could be managed conservatively in the acute phase. Only 25% of these patients required surgery at a later stage. They recommend emergent esophagectomy only for patients with extensive necrosis (stage 3b).64 Laparotomy may be needed for an evaluation of the depth of injury in some patients with extensive second or third degree injury. It also provides the option for the placement of a feeding gastrostomy tube and a continuous #4 silk suture, which may be utilized for retrograde dilation should it become necessary at a later date.

Treatment during chronic phase In patients with severe esophageal injury, strictures typically develop within 3 to 4 weeks. Earlier frequent dilation serves to minimize this risk.76 A barium esophagogram should be obtained at this time to assess the degree of stricture formation, the site of strictures, and contour of esophageal lumen. A solid bolus challenge may be required for accurate assessment if no stricture is apparent with liquid barium. A detailed regimen of wire-guided esophageal dilation needs to be planned as outlined above in the section on DIED. The dilation strategy should, however, take into account that the transmural fibrosis seen in this condition makes the esophageal wall prone to tearing and perforation. These patients may have pseudodiverticulum formation and require a much more careful approach. It is prudent to begin with a dilator size just below the estimated lumen diameter (by barium esophagogram) and advance only one or two millimeters in dilator diameter in the beginning. The rate of dilator size progression is determined by the resistance encountered, as well as operator experience. Some authors have shown a decrease in the need for repeated dilation when intralesional injections of triamcinolone were used in both pediatric and adult population.38,39 The mechanism by which

247 batteries are less than 15 mm in diameter, with 62.5% being 11.6 mm in diameter (range 7–23 mm).79–81,83 Disc batteries should be considered as a foreign body with severe corrosive properties or a corrosive chemical delivered as a small pellet. Contrary to early belief, Litovitz did not find the severity of injury to be dependent on the electrical status of the battery in a study of 1718 cases in which the battery status and outcome were both known. Instead, they found that lithium batteries with their larger size and higher voltage (3 volts) were associated with more severe damage.

Detection and treatment of late complications Prevention As discussed above, patients with a history of corrosive injury to their esophagus have been estimated to have a 1000 times higher incidence of squamous cell carcinoma.57,58 It may thus be reasonable to perform periodic surveillance endoscopies with Lugol staining chromoendoscopy in these patients starting 15 years after injury. However, no studies are available to prove or disprove the usefulness, cost-effectiveness or the proper interval of endoscopic surveillance.

TREATMENT ISSUES SPECIFIC TO MINIATURE (BUTTON) BATTERY INGESTION Introduction The ingestion of ‘button’ batteries follows the old axiom that ‘toddlers put in their mouth what they get their hands on.’ ‘Button’ battery ingestion represents a relatively new phenomenon. These miniaturized alkaline batteries have rapidly replaced the older cylindrical cells (Fig. 16.1). With electronic toys and quartz watches replacing their mechanical counterparts, these batteries are present in every modern household. They contain a highly concentrated solution of potassium or sodium hydroxide and potentially toxic compounds of mercury and zinc, lithium and cadmium. Over a 10-year period (1982–1992), 2320 cases of button battery ingestion were reported to the National Button Battery Ingestion Hotline at Georgetown University Hospital’s National Poison Center (202-625-3333).79–81

Pathogenesis

Precautions required to prevent ingestion of button batteries are similar to those needed for any foreign body ingestion. However, due to their potential for causing rapid damage, it is extremely important to keep these batteries out of reach of children. Sixtysix percent of battery ingestions occur in children younger than 6 years of age.79–81 Children who use a hearing aid require closer supervision because nearly one-half of the reported ingestions involve these batteries. Education of audiologists, parents, and children may help reduce these events. Design improvements and industry involvement can likely eliminate this threat. It may be prudent for the manufacturers to use smaller batteries, which are less likely to get impacted in the esophagus. Further miniaturization and the development of batteries that do not contain corrosive materials may eliminate this damage in the coming decades. The development of one such battery was reported in the lay press by researchers at Johns Hopkins University.

Management Foreign body identification Prompt identification and location of the battery is the most important first step in this condition. Once a possible case is brought to the notice of a physician, posteroanterior and lateral chest radiographs should be promptly obtained. A ‘double-density’ opacity is usually produced by a disc battery.84 The edges of a battery are more rounded than that those of a coin. An abdominal radiograph is also indicated initially to search for other foreign objects that may have been ingested.

Removal

The major mechanism of injury to the esophagus is the leakage of the caustic alkaline solution from the button battery. Esophageal mucosal damage may occur within 1 hour of ingestion, and the degree of damage correlates directly to the duration of contact with the mucosa.82 The risk of impaction of a disc battery in the esophagus depends on its size, being more likely with batteries larger than 20 mm in diameter. Fortunately, 97% of the ingested

If the battery is lodged in the esophagus, a prompt endoscopic extraction is mandatory. No neutralizing agents have been found to be useful to prevent or decrease esophageal damage while the patient is in transit to a medical center.85 Emetic agents are generally ineffective and should not be used. Although Foley catheter balloon-assisted removal of foreign bodies is considered safe in patients with a disease-free esophagus, this method is not

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11 mm

17 mm

18 mm

21 mm

24 mm

Fig. 16.1 A photograph of an 11 mm disc battery and common coins, showing the rounded edges of the battery that make its retrieval using forceps difficult.The caustic material leaks out from the gap between front and back covers. The coins have elevated edges, which enable them to be grasped with alligator/rat-tooth forceps.

Treatment Issues Specific to Miniature (Button) Battery Ingestion

intralesional steroids benefit in this condition is not clearly understood. Often patients not properly treated by adequate dilation early in the chronic phase, or who are later neglected during follow-up, will require a series of careful dilation sessions to achieve and sustain adequate esophageal patency. Collagen synthesis inhibitors may have a role in this condition; such agents, however, are currently under investigation and no data presently support their use.78

Treatment of Esophageal Disorders caused by Medications, Caustic Ingestion, Foreign Bodies and Trauma

248 recommended for disc batteries due to a lack of control.86–88 The use of a magnetic probe for the removal of button batteries has been reported in European countries.89 A protocol for the management of ingested button batteries is presented in Table 16.6. Most reviews do not recommend any intervention for batteries that have arrived in the stomach or more distally at the time of diagnosis.88–90 However, more recent experience tends to suggest that polyethyline glycol solution preparations may be used safely to flush the battery more quickly.91

Endoscopic intervention Oral removal by endoscopy is the treatment of choice for button batteries lodged in the esophagus. General anesthesia or monitored anesthesia care with protection of the airway may be required in infants and children, while adolescents and adults may be able to undergo endoscopy using intravenous sedation. A bronchoscopy prior to endoscopy should be performed if more than 4 hours have elapsed since the ingestion of battery to identify a fistula that may form as a result of full-thickness injury to the anterior esophageal and posterior tracheal walls. Endoscopic removal of disc batteries from the esophagus is challenging. General principles employed in the removal of disc batteries are similar to those followed for any other foreign body retrieval with the exception of need for removal as early as possible (Table 16.7). Because of their rounded edges, these batteries are difficult to grasp securely with foreign-body forceps or snares. If the exact size and type of the battery is identified, the choice of instrument can be made by prior rehearsal. Common US coins and a disc battery are shown in Figure 16.1. Forceps with magnetic properties may be more useful in these situations, but are not currently available. An overtube may be used to protect the airway or to prevent dropping the battery as it traverses the cricopharyngeal sphincter. A Dormier basket as used for gallstone retrieval

Table 16.6 Management protocol for esophageal button battery History: establish accurate size and time of ingestion Initial X-ray (posterior-anterior and lateral chest X-ray plus abdominal X-ray) Esophageal battery: emergent endoscopic retrieval Identify the chemical system: mercury levels only when battery disintegrated For help call (202) 625-3333 in the United States or contact your physician immediately

Table 16.7 Indications for emergent removal of ingested foreign body Respiratory distress Foreign body at the cricopharyngeus level

or the Roth Retrieval Net used to retrieve colon polyps may be helpful. Only 33% of attempted removals have been reported as successful.81 If retrieval is not possible, the battery can be gently pushed into the stomach and removal attempted from the stomach. However, this maneuver should only be done if the lumen beyond the battery is clearly visible, adequately patent, and free of any pathology. If retrieval is not possible even from the stomach, the battery should be left in the stomach and a follow-up radiograph obtained at 48 hours to follow the passage of the battery. Although Willis and Ho reported the perforation of a Meckel’s diverticulum by an ingested disc battery, no further intervention is generally required if the battery has passed beyond the pylorus by 48 hours and if no symptoms are reported.90

Role of surgery Early surgery may be indicated if a perforation, full-thickness injury, or fistula formation is detected by endoscopy and/or bronchoscopy. The management is then the same as that of perforation due to any foreign body.

Post-retrieval measures If a battery has been removed uneventfully without full-thickness damage evident on endoscopy, no further intervention may be required. In patients where progression to full-thickness burn or fistula formation may be likely, a barium swallow using thin barium may be performed during the next 24–48 hours. This study may be repeated in the next several days to delineate stricture formation. Treatment with proton pump inhibitors or sucralfate may be useful if mucosal erosion is seen. The use of laxatives or prokinetics to promote the passage of a gastrointestinal button battery is not recommended since most batteries are excreted within 72 hours.88

ESOPHAGEAL FOREIGN BODIES (NONFOOD) Foreign body ingestion results in approximately 1500 deaths annually in the United States. A large majority of foreign body ingestions occur in children, edentulous elderly, prisoners, and psychiatric patients. In a recent series of 414 adult patients with ingested foreign bodies, 38% were nonfood-related objects. Seventy-five percent of these objects were found in the esophagus (36% cervical, 19.8% mid-esophagus, and 19.1% distal esophagus).92 Nonfood foreign bodies are ingested primarily by children.93 These include coins, components of toys, crayons, and small household items such as pens, paper clips, and safety pins. College students have a propensity for accidental ingestion of coins as a consequence of a flip and oral catch game often played under the influence of alcohol. Prisoners, on the other hand, have been reported to indulge in recurrent (3–10%), deliberate ingestion of many types of foreign bodies for secondary gain.95,96 Nearly 75% of all documented ingested foreign bodies are lodged in the esophagus at the time of diagnosis.97

Inability to swallow secretions Evidence of perforation Button battery ingestion Sharp object ingestion

Pathogenesis Children ingest foreign bodies while playing with them, while the elderly who ingest foreign bodies most often have their palatal

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Prevention of foreign body ingestion is far more cost-effective than their extraction. Coins and small objects that can be swallowed should be kept out of the reach of infants and small children. A similar strategy for close supervision should be adopted for the mentally retarded and elderly patients.

reported to be 100% successful in a small number of patients. This approach may represent a simple strategy, but its safety and efficacy needs to be further tested by a larger study.103 Other effervescent agents that release large quantities of CO2 upon ingestion have also been used, with success rates of 75%.104 However, because effervescent agents in the setting of complete obstruction have resulted in perforation, their use can not be recommended. Their use may be safe prior to endoscopy in patients with nontoxic, blunt/round, small-caliber foreign bodies in the absence of preexisting esophageal pathology. A technique usually reported by radiologists and not favored by most gastroenterologists involves the use of a Foley catheter for the removal of esophageal foreign bodies. This technique has been widely reported in emergency medicine and in the pediatric literature and employs the passage of a Foley catheter under fluoroscopic guidance, followed by inflation of its balloon distal to the ingested object.105–107 The catheter is then withdrawn, thus removing the foreign body. This technique has been shown to be safe in the pediatric population, where pre-existing esophageal pathology is generally not encountered. The technique has an obvious cost advantage because it obviates the need for an endoscopy and minimizes the period of observation in a hospital or emergency room. The primary risk of this strategy is the lack of control when the object passes the hypopharynx. This risk may be overcome either by the use of endotracheal intubation or placing the patient in a Trendelenburg position. In a survey of pediatric radiologists, Campbell and colleagues reported 2500 successful foreign body removals, with only one complication.108 The use of this method is limited to blunt objects within 12 hours of ingestion.105 Gastroenterologists prefer endoscopy over the Foley balloon catheter, perhaps due to their experience with endoscopy and lack of experience with Foley catheter technique.94,109 Because esophageal disease is so common in patients with esophageal foreign bodies, an endoscopy should be performed in all cases. The blind passage of an esophageal bougie to push the foreign body into the stomach has been described, but should not be done because of the high risk for perforation and the ready availability of safer alternatives.110 Thompson and colleagues recently described another nonendoscopic technique for the removal of gastric and esophageal metallic foreign bodies, using a magnetic orogastric tube.111,112 Although their reported success rate was >90%, lack of control is once again an issue. The technique, however, has the potential of being useful as an adjunct to endoscopy and overtube placement.

Removal of esophageal foreign bodies

Endoscopic removal

Diagnosis A history of definite ingestion by the patient/witness or in its absence other associated signs of dysphagia, odynophagia, sialorrhea, chest discomfort, or constitutional, signs of perforation may all point to the diagnosis of foreign body ingestion. Radiography is of paramount importance as most ingested foreign bodies are radiopaque. Since 1982, at the insistence of pediatricians and radiologists, all North American coins have been minted with radiopaque metals.98 It is important to obtain two axis (AP and lateral) views to estimate the exact location, size, and shape of the object. However, plain films have false-negative rates up to 47% in the detection of foreign bodies.99 When the suspicion is strong, but plain radiography fails to identify a foreign body, barium contrast radiography is often useful. However, barium should be avoided in patients suspected to have total esophageal obstruction. Also, barium may be retained in enough quantity with incomplete obstruction to hinder endoscopic examination. Radiographic diagnosis assists the endoscopist in planning the procedure and selecting the timing and equipment for retrieval.94,97 It may also rule out or confirm a suspicion of perforation. CT scanning of the neck and chest with soft tissue and bone windows provide better contrast and are more useful in foreign body detection.100 Flexible video endoscopy has the advantage of combining diagnostic and therapeutic capabilities. Extreme care should be exercised by the endoscopist during the procedure. It is critical that the passage of the endoscope and accessories be done under constant direct vision and never blindly into or beyond a foreign body.

Prevention

Nonendoscopic management In a retrospective study of esophageal foreign bodies, Crysdale and colleagues101 reported that 7.8% passed spontaneously within 24 hours, while another 2.5% passed with the use of pharmacological agents. In contrast, Tibbling and Stenquist reported a spontaneous passage rate of 21% within 24 hours,102 which further increased to 29% if endoscopy was delayed beyond 24 hours. Spontaneous passage is almost universal once the foreign body has reached beyond the lower esophageal sphincter. Nonendoscopic approaches can be divided into two categories: those that promote the passage of the object distally and those aimed at extraction of the object. Distal passage is promoted primarily by pharmacological means using agents that relax the lower esophageal sphincter. The use of a carbonated drink has been

Rigid esophagoscopy was most widely used for foreign body removal prior to the 1960s and 1970s. However, the availability of flexible fiberoptic endoscopes, and more recently video endoscopy, has brought about a revolution in this field. The diameter of the endoscopes has become progressively smaller, thereby making flexible endoscopy favored for the removal of foreign bodies. Gastroenterologists today are primarily trained in, and prefer to use, flexible video endoscopes, a preference that is widely supported.93–95,97,113 In his report of 242 foreign body removals, Webb used a flexible endoscope in 211 (87%) cases.93 Similarly, in a 15-year review of foreign body management, Weiss and colleagues employed flexible endoscopy in 111 of the 132 cases where endoscopic removal was carried out, with a success rate of 90%. In addition, flexible endoscopy has the advantage of being safer, with a reported perforation rate less than one-half that of rigid esophagoscopy (0.9%

Esophageal Foreign Bodies (Nonfood)

sensation reduced or eliminated by a denture plate. One such example is the aluminum foil wrapping on medications with the medication enclosed, which has resulted in esophageal perforation. Although uncommon in children, adults who have esophageal foreign bodies impacted in the esophagus have underlying lesions of the esophagus in up to 88% of cases.95

Treatment of Esophageal Disorders caused by Medications, Caustic Ingestion, Foreign Bodies and Trauma

250 versus 2%).95,110 Rigid endoscopy retains a role for the removal of foreign bodies impacted in the hypopharynx and cricopharyngeus (upper esophageal sphincter) and in those not removable by a flexible endoscope.

Table 16.8 Esophageal foreign body

Suitable extraction accessories

Preparation for endoscopy

Coin

Roth net, alligator forceps, rat-tooth forceps, snare, basket,TTS balloon, magnetic probe (if available)

Button battery

Roth retrieval net, Dormier basket, magnetic probe

Thumb tacks

Alligator forceps, rat-tooth forceps

Sharp objects (pins, needles, toothpicks, blades, open safety pins, fish bone)

Overtube, hooded sheath, snare, alligator forceps

Marbles, seeds, eraser

Baskets, snare, polyp retriever

Food bolus (meat)

Overtube Stiegman-Goff adaptor, Dormier basket

Indications for emergent foreign body retrieval are summarized in Table 16.7. While performing endoscopy for removal of foreign bodies, one must ascertain that the patient is completely cooperative or adequately sedated and properly monitored, with ample assistance and equipment available to the endoscopist. If intravenous conscious sedation does not achieve this objective, monitored anesthesia care (MAC) using short-acting intravenous agents, such as propofol, is preferred. MAC is especially useful when endotracheal intubation is required for airway protection. Availability of the surgical team, if needed, should be ascertained before beginning any foreign body removal, especially when dealing with sharp object or button battery ingestion or when the object was ingested more than 24 hours previously.

Equipment selection Most experts in this field practice and recommend a proper selection of equipment and planning (i.e., a ‘dry run’), using accessories to practice grasping a similar foreign body prior to the actual procedure.94,97 This process provides the endoscopist and the endoscopy assistant a feel for both the eventualities that might occur during the retrieval and the suitability of the accessory equipment to be used.

Accessories Various accessories have enhanced the ability of the endoscopist in successful retrieval of ingested foreign bodies safely (Table 16.8). These include: overtube, alligator forceps, rat-tooth forceps, (both manufactured by Olympus America Inc., Lake Success, NY), Roth retrieval net, (US Endoscopy Group, Inc., Mentor, Ohio), polypectomy

snare, Dormier basket, tripod, hooded sheath, and the StiegmanGoff adaptor for variceal band ligation (Figs 16.2–16.4). Of these, the plastic overtube is a versatile, multipurpose accessory that should be stocked in every endoscopy unit (Fig. 16.2). It also allows multiple passages of the endoscope with lesser patient discomfort. When back-loaded on an endoscope and advanced after the endoscope tip is beyond the cricopharyngeus, it can be advanced over the scope to provide airway protection. However, injury can occur due to trapping of the mucosa between either an endoscope or a Maloney dilator used as an obturator to introduce the overtube.114 Introduction of the overtube should be performed gently and carefully regardless of the obturator (endoscope or rubber bougie) used. A 44 French size Maloney dilator is used as the obturator for

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Overtubes. Fig. 16.2 (A) Conventional, black, straight overtube with sharp inner edge; (B and C) Newer variety, curved, clear plastic (20 cm long) overtubes. Note their round (B) and tapered (C) distal ends. (D) Friction tip (Stiegmann-Goff) adaptor for variceal ligation and meat bolus extraction.

A

B

C

D

251

A

B

C

D

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A dual exposure Fig. 16.4 photograph showing: (A) rat-tooth forceps, (B) alligator forceps, and (C) alligator forceps with rat-tooth jaws.These accessories are useful in removal of a variety of foreign bodies.

A

B

C

passing one standard model of overtube in patients without esophageal foreign bodies; however, this blind overtube passage should not be used for fear of push injury when an esophageal foreign body is suspected. Sharp objects, such as pins, needles, blades and wires, can be withdrawn into the tube, thus protecting the esophageal mucosa from damage. Coins, the most common foreign bodies ingested by children, are best removed using an alligator or a rat-tooth forceps or a Dormier basket (Figs 16.3, 16.4). These forceps have sharp jaws that appose well to grasp an object

with rough and vertical edges. Button batteries, on the other hand, have rounded edges that are difficult to grasp with forceps. In an in vivo comparison of various accessories, Faigel and colleagues demonstrated that button batteries could be removed only by using either a basket or a Roth Retrieval Net (Fig. 16.3), whereas the snare was the best instrument for removing toothpicks and thumb tacks.115 A through-the-scope (TTS) balloon may at times be used to remove a foreign body under direct visualization via a two-channel operating endoscope, or as

Esophageal Foreign Bodies (Nonfood)

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Photograph showing: Fig. 16.3 (A) Snare, (B) Roth Retrieval Net, (C) polyp retriever, and (D) Dormier basket.

Treatment of Esophageal Disorders caused by Medications, Caustic Ingestion, Foreign Bodies and Trauma

252 a means of opening the lumen distal to a foreign body in the grasp of a snare or forceps.

Body packer syndrome (cocaine-loaded foreign body) The popularity of cocaine as a recreational drug within the United States has resulted in increased smuggling of this drug across international borders. Its abundant availability in South American countries and the enormous cost difference between these countries and United States has resulted in people devising ingenious ways to smuggle the drug. ‘Body packing’ or ingesting cocaine-filled latex condoms is one such ingenious method used to conceal the illicit material. Each pack generally contains up to 5 grams of cocaine. Once the ‘packer’ arrives at his destination, the ingested pack is retrieved after it is passed in feces. The clinical significance of this crime strikes home when the scheme does not proceed as planned. Complications of this ingestion usually arise when the packages rupture or are not passed in the feces within 24–48 hours. Esophageal impaction with these packages is rare, but may occur as with any ingested foreign bodies. Johnson and Landreneau reported a case of esophageal obstruction and perforation due to ingested marijuana packs by a prisoner in Missouri.116 The cocaine/drug packs are unique in that endoscopic removal should not be attempted because it may lead to perforation of the pack and release of a fatal dose of the drug. Whenever detected, these packs are best managed surgically. The general condition of the patient merits intensive observation and supportive care if some or all of the packs have traversed the esophagus.

TREATMENT OF FOOD BOLUS IMPACTION Introduction A food bolus represents a specific type of foreign body, and most studies deal with the accidentally swallowed, unchewed or unprepared food bolus as a part of ingested foreign bodies. We deal with the specific aspects of management of food bolus separately due to the unique characteristics of this foreign body. Impacted food bolus is the most common type of foreign body encountered in adults. In a large majority of cases, a food bolus impacts in the esophagus due to an underlying disorder. The impacted food is usually a piece of meat that is swallowed without careful chewing. Hence, the commonly used terms include ‘meat impaction’ or ‘steakhouse syndrome.’

Pathogenesis A distal esophageal ring or a stricture is usually present that prevents the passage of the bolus into the stomach. Patients frequently present several hours after dining at a restaurant or having a big holiday meal. Meat boluses impacted for over 12 hours or those that contain slivers of bone create a higher risk for esophageal perforation during attempts at removal.

Diagnosis/treatment As discussed in the section on foreign bodies above, diagnosis is often apparent from the history. Most patients receive glucagon,

nitroglycerine, or similar medications in the emergency room before a gastroenterologist is consulted. The statistics presented above for success of these agents in foreign bodies are applicable to the impacted food bolus. Recent experience with glucagon has not been very gratifying. Although esophageal perforation was reported with the use of papain as early as 1968,117 the use of meat tenderizers (a very reduced concentration of papain) was common in emergency rooms long after that.118 The use of this agent should no longer be considered a standard treatment. Papain, the active ingredient in meat tenderizer, has no effect on normal mucosa, but contact with inflamed mucosa may incite a marked increase in inflammation,117 and mural digestion may occur if the tissue is ischemic. Because of its chemical nature and contact with saliva, a food bolus impacted in the esophagus undergoes progressive degradation with passage of time. This feature is of importance in planning its extraction. If the patient can handle salivary secretions, emergent endoscopy is not necessary. Observation and sedation may allow spontaneous passage of the food bolus.93 If urgent endoscopy is performed, a meat bolus ingested recently can potentially be extracted in one piece using a snare or a basket. However, if more than 12 hours have elapsed since the consumption of the meal, the meat may have become very soft and fragmented. Under such circumstances, multiple passages of the endoscope may be required, necessitating the use of an overtube.94 The standard forceps and snare accessories often are inadequate for removing such impactions. Saeed and colleagues in 1990 reported the use of the StiegmanGoff band ligator tip as an accessory for meat bolus extraction (see Fig. 16.2D).119 This technique produces a suction cup at the tip of the endoscope, thus facilitating removal of a soft food bolus. Despite disintegration with the usual instrumentation, the bolus can be suctioned and anchored into this cup during the passage across the cricopharyngeus. Homemade endoscope tip adaptors fashioned from plastic tubing were, however, in use even prior to this report. The newer variety transparent variceal band ligator adaptors are even more suitable for this task as they do not occlude the endoscopist’s field of vision. Other aspects of meat bolus extraction are generally identical to those of ingested foreign bodies. Any bolus that completely occludes the lumen and prevents visual inspection of the lumen beyond the bolus should not be blindly pushed ahead with the endoscope or any accessory instrument because of an increased risk of perforation.

Treatment of the underlying disorders An underlying esophageal structural abnormality is present in up to 80% of adults with foreign body impaction in the esophagus. An appropriate therapy of the underlying lesion may thus prevent future recurrences. The lesion most often encountered is a refluxinduced esophageal stricture. Mosca et al. found associated pathology in 83 (30.7%) of their patients (stricture, 50; hiatal hernia, 11; achalasia, 11; and Schatzki ring, varices, diverticula, and cancer, 11).92 If the ingested object or food bolus is present for more than 12 hours and the esophageal mucosa shows signs of ischemia/ inflammation, esophageal dilation should be deferred for at least 1–2 weeks after foreign body removal. A malignant lesion should be appropriately managed. Patients with psychiatric disorders should receive prompt help via psychiatric consultation and should be appropriately treated because of the risk of repeated ingestion or other suicide attempts.

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Introduction Traumatic injury to the esophagus can be classified into two groups based on etiological mechanisms. The first and far more frequent is the extrinsic group, which includes instrumentation, such as endoscopy, dilation, surgery, foreign bodies, and thermal ablation of lesions. Recognition of complication risk and efforts at prevention are the key elements in avoiding perforation.120 The second and less common group is due to intrinsic causes, which includes MalloryWeiss tear, Boerhaave’s syndrome, and malignant strictures.

Pathogenesis Various etiological factors involved in trauma to the esophagus are summarized in Table 16.9. Instruments such as endoscopes, bougies, hydrostatic or pneumatic balloon dilators, guidewires, tips of hydrostatic (TTS) dilators, and other accessories all may cause disruption of the wall of the esophagus due to a shearing or radial force or a direct puncture. Owing to its unique anatomic characteristic of lacking the serosal layer, the esophagus is especially susceptible to these forces. Trauma during or after surgery, on the other hand, may be either direct laceration or disruption of vascular supply at the time of surgery resulting in an ischemic injury, which finally results in perforation. Modalities such as thermal lasers, multipolar coagulation and heater probe, or photodynamic laser therapy (PDT) may traumatize the esophagus by direct burn

or deep desiccation, which eventually results in necrosis of the tissue and perforation. Barotrauma or forceful distention may take place due to excessive insufflation of air during various procedures, especially in the setting of complete obstruction.

Prevention Esophageal injury due to instrumentation may increase as newer procedures, instruments, and techniques are adopted for achieving hemostasis and performing esophageal dilation, as well as with the advent of endoscopic antireflux procedures. In our view, adequate emphasis on prevention of iatrogenic injury is likely the most important part of management. The following section deals with issues important for the prevention of iatrogenic esophageal injury.

Barium esophagogram

Table 16.9 Esophageal trauma: etiology

‘Cost containment’ issues have also resulted in the endoscopist often not having the luxury of, or making the effort to, obtain a barium esophagogram study prior to endoscopic intervention for stenotic lesions. Identification of pre-existing lesions prior to endoscopy by barium swallow is, however, useful. The value of a barium esophagogram being available prior to endoscopy in stenotic lesions of the esophagus cannot be overemphasized. A detailed history may help in selecting the cases where a barium study must be obtained before endoscopy is attempted. A barium esophagogram helps to identify the site, length, and contour of the stricture. It also alerts the endoscopist to the possibility of more than one stenotic lesion with different characteristics being present in one patient. A barium study will identify necrotic cavities in an esophageal carcinoma prior to endoscopy, dilation, or stent placement that otherwise might be interpreted as a perforation when done following the procedure.

Extraluminal etiologies Penetrating wounds

Issues relating to fluoroscopy, wire guidance and TTS balloons

Blunt trauma Operative injury Through-the-wall suture Disruption of blood supply Laparoscope/other instruments Intraluminal etiologies Intrinsic Mallory-Weiss tear Boerhaave syndrome Esophageal malignancy Ulceration Extrinsic Foreign bodies/nonendoscopic instrumentation Bone/pin ingestion, endotracheal, nasogastric, orogastric tube placement Endoscopic instrumentation Dilation, guidewire/endoprosthesis placement, balloon tip Pneumatic dilation, sclerotherapy, laser or electrocoagulation, overtubes

Several developments in the evolution of endoscopy have resulted in esophageal dilation being done routinely without the use of fluoroscopy. These include time constraints, commercial promotion to employ newer TTS balloons for esophageal dilation, the demonstrated safety of esophageal dilation in simple, distal, peptic strictures without the use of fluoroscopy, and the advent of officeor outpatient center-based endoscopy. All have led to the general belief that fluoroscopy may be superfluous for most esophageal strictures. However, fluoroscopy helps in completing a safe, effective dilation of esophageal stricture and is of utmost value when the endoscopist is not familiar with the severity of the lesion. We prefer that patients be in a supine position for this procedure, especially when using fluoroscopy, which helps in the correct anatomical identification of landmarks and helps in following the course of the dilator accurately. Availability of excellent C-arms with digital image quality has brought fluoroscopy out of hospital radiology departments and into modern endoscopy units, thereby making it easily accessible. Esophageal dilation under wire guidance has made esophageal dilation safer and, in the authors’ view, should be the method of choice for most dilation procedures. The wire placement should either be endoscope assisted or under fluoroscopic guidance or both. Advancement of the Savary wire or a thinner, floppy wire under fluoroscopy may prevent inadvertent injury when a patient has

Traumatic Injury to the Esophagus

TRAUMATIC INJURY TO THE ESOPHAGUS

Treatment of Esophageal Disorders caused by Medications, Caustic Ingestion, Foreign Bodies and Trauma

254 luminal abnormalities, such as a Zenker diverticulum, cricopharyngeal bar, epiphrenic diverticulum or large hiatal hernia. The Savary wire, although flexible at its tip, has been reported to cause perforation of the gastric or duodenal wall when not fixed diligently in position during advancement of the dilator. Injury occurs when the flexible tip is completely flexed or the wire bent acutely, and force is exerted either at the junction of the flexible tip and stiff steel wire or against the point of the bent wire. Due to its thickness and relative rigidity, the tip may also traverse severely inflamed, friable tissue planes if not observed carefully during endoscopy or under fluoroscopy. Esophageal TTS hydrostatic balloons have gained increased popularity in recent times for the dilation of esophageal strictures. Although far more expensive than bougie-type dilators, aggressive marketing and relative ease of use form the basis of their increased usage. These balloons, however, have a long, semi-firm tapered tip, which is often several centimeters away from the view of the endoscope (Fig. 16.5). The tip is prone to causing injury to the mucosa in the presence of inflammation, friability, or carcinoma, especially when the endoscope is being repositioned or with respiratory excursion. This possibility is even more important with longer balloons or when a stenotic lesion does not allow the passage of the endoscope to direct safe passage of the balloon dilator tip. The tip should be carefully observed at the time of advancement and at every point when the balloon or the endoscope is advanced. Development of an even more flexible tip may address this problem. Regardless, the endoscopist and the assistant need to diligently fix the endoscope at the mouth and the balloon catheter at the insertion port of the endoscope, which should prevent inadvertent movement of the balloon dilator or its tip during inflation. Another concern is the use of these hydrostatic balloons to dilate strictures due to causes likely associated with deep transmural injury and fibrosis, such as those related to radiation and caustic injury. In our opinion, wire-guided dilation or Maloney dilators under fluoroscopic control are safest in these patients.

Issues relating to thermal or other ablative modalities Adhering to safe levels of power settings while performing thermoablation procedures and becoming familiar with new equipment prior to use may prevent accidental deep burns. Testing the power settings in vitro on comparable animal tissue or in vivo in the stomach (which has a thicker wall) immediately before use may prevent deeper esophageal burns or perforation. Using lower power settings when the tissue is inflamed or treating raised lesions and avoiding excavated lesions may also be helpful. The depth of ablation achieved with equipment made by different manufacturers may differ even with similar settings. Early experience with the radiofrequency technique for treatment of gastroesophageal reflux (STRETTA™) has reportedly resulted in perforation, although added experience has improved its safety profile. The Endo Cinch™ device technique has recently been reported to have caused a perforation of the distal esophagus that was managed laparoscopically.121 It is obvious that these techniques are best used by adequately trained operators who perform these procedures regularly.

Issues relating to overtubes and foreign-body removal During endoscopy, intubation and advancement of the endoscope should be done under direct visualization. While attempting foreign body retrieval, the overtube should not be passed until the foreign body and esophageal mucosa have been examined. The use of an overtube should be avoided if possible, but not at the cost of compromising the airway. However, overtubes are important in the protection of the airway and should be used when indicated. Mucosal injuries related to passage of overtubes can be minimized by placing the overtube in warm water prior to insertion and passing the overtube over a proper diameter bougie.122,123 The largest bougie that can be comfortably moved in and out of the overtube should be used. The use of the newer variety 60F/20 cm length tube with a filed, blunt, rounded leading edge may further reduce this trauma.124 Inadequate sedation and inability of the assistant to hold the overtube in place are two factors that may precipitate accidental,

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Fig. 16.5 Photograph showing tip of a TTS balloon.The tip (arrow) can traverse through inflamed, necrotic, or even normal tissue, with sufficient force, during blind placement and cause perforation if caution is not exercised.

255

Management of perforation of the esophagus Causes of esophageal perforation have been listed along with causes of esophageal trauma in Table 16.9. Whatever the cause, esophageal trauma and perforation constitute an emergency and require rapid diagnosis and treatment. The signs and symptoms usually depend on the cause, location, and extent of perforation (Fig. 16.7). Patients usually present with tachycardia, chest pain, shortness of breath, and vomiting, and may have subcutaneous or mediastinal emphysema. Efficient management of esophageal perforation begins with an accurate history in high-risk cases. The classic scenario is of a patient presenting after consuming a large meal that includes alcohol, followed by vomiting and/or severe bouts of coughing, chest pain, and dysphagia. Subtle presentations may include a history of consumption of carbonated drinks/beer with forceful retching, blunt trauma to the chest during a fist fight or accident, swallowing a sharp bone or object, or severe coughing episodes. Symptoms of pleuritic chest pain with radiation to shoulder, neck or jaw, or epigastric pain in a patient with the abovementioned history should alert physicians to the possibility of esophageal perforation. This possibility is especially important for the physicians evaluating patients during the night or in walk-in

clinics, where several hours may elapse before the patient is likely to be seen by another physician. Early detection and evaluation of suspicious symptoms with chest radiographs and barium esophagogram can be invaluable in improving the eventual outcome. Radiographic studies may show subcutaneous emphysema (Fig. 16.8), mediastinal widening, pneumothorax, pleural effusion, or an air–fluid level in the mediastinum. Typically, a water-soluble contrast (Gastrograffin®, meglumine diatrizoate) swallow should be performed if esophageal perforation is suspected. This study should be the first radiographic procedure done for the evaluation of a suspected perforation after a PA and lateral chest X-ray. If negative, a barium esophagogram using a limited volume of thin barium is more likely to reveal small perforations and should be done. If perforation is still suspected, a CT scan will prove most sensitive for revealing barium outside the esophageal lumen. Once esophageal perforation is suspected, regardless of whether initial studies are negative, a thoracic surgeon with significant experience in performing esophageal surgery should be contacted promptly. Preferably, the surgeon should be alerted to the possibility of esophageal perforation and be available on call even before a relatively high-risk procedure, such as pneumatic balloon dilation for achalasia, is actually performed. The patient with suspected esophageal perforation is best managed in the hospital under close observation with surgical consultation until perforation is excluded. Nontransmural tears of the esophagus can be successfully managed conservatively and patients discharged within 3 to 4 days.125 Occasionally, limited/nontransmural tears may extend after delayed weakening of the wall by infection or by high intrathoracic pressures generated by gagging, vomiting, or coughing. Thus, the diagnosis should be reviewed and diagnostic studies repeated if the clinical condition of the patient does not improve rapidly. Esophageal perforation occurring after endoscopy or dilation is considered by some authors to represent a different entity. Although surgery forms the mainstay of therapy, several studies have reported successful management of these patients by conservative

•

Fig. 16.6 Photograph showing the cut internal bumper of a gastrostomy tube.The relatively sharp tube end can cause mucosal injury. Retrieval direction (arrow) should be with the sharp end trailing.

Traumatic Injury to the Esophagus

uncontrolled, and repetitive repositioning or advancement of the overtube, thereby increasing the chances of mucosal injury. The older, larger, longer, and stiffer overtube (see Fig. 16.2A) should be considered obsolete and removed from the endoscopy units. As described above, while removing foreign bodies, the sharper end should always be trailing (Fig. 16.6) in order to avoid accidental puncture of the mucosa. Removal of a PEG tube mushroom should be done by the external traction method whenever possible. Cutting of the internal bumper and snare-assisted retrieval should only be done when one-step external traction removal is not possible. If not retrieved carefully, these bumpers can result in esophageal perforation.

Treatment of Esophageal Disorders caused by Medications, Caustic Ingestion, Foreign Bodies and Trauma

256

•

Algorithm for management of Fig. 16.7 esophageal perforation.

Possible etiologies Endoscopy Dilation Intubation Trauma

Vomiting Foreign body Caustic ingestion

Symptoms and signs suggest perforation Pain – chest, neck, abdomen *Tachycardia, dyspnea, hypotension, fever, subcutaneous emphysema Assure availability of or consult with experienced esophageal surgeon

Admit for evaluation and observation

Establish IV access

PA-lateral radiographs chest, neck, abdomen

Diagnostic of perforation

Water soluble contrast esophagram

Negative

Decision for surgery vs. medical therapy

Diagnostic of perforation

Barium esophagram (thin, small volume)

Diagnostic of perforation

Negative

CT chest

Overnight hospital observation

treatment, using intravenous fluids and antibiotics.126–131 Mortality is generally low compared to noniatrogenic patient groups, although morbidity is higher in patients with delayed (>24 hours) identification of perforation.132 If the patient is not a surgical candidate and has a limited life span, as in patients with esophageal cancer, immediate placement of a plastic or coated metal expandable endoprosthesis is an option, with 60–90% chances of survival.133,134 Despite these reports, it must be emphasized that such patients require close observation, preferably in the intensive care unit, aggressive supportive care, broad-spectrum antibiotic therapy and an alternative source of nutrition. Surgery should be considered if clinical improvement does not continue. There has been one case report where perforation following pneumatic balloon dilation for achalasia was treated endoscopically using a metallic clip.135 In the future, laparoscopic surgery may also play a larger role in the management of small, clean, iatrogenic perforations that are detected early.120 Perforation due to noniatrogenic trauma is best managed by early surgical repair.136 Historically, patients undergoing early surgery

Negative

have had a better outcome. Mortality rates as high as 56% with delayed recognition of esophageal perforation are reported.137,138 More recent reports, although maintaining the trend of poor prognosis for patients with delayed detection, show a comparatively better outcome in both groups.139 Most patients are able to avoid esophagectomy. Some of these studies also support conservative management for noniatrogenic perforations. The studies that have evaluated a conservative approach for this group of patients report success in patients with hypopharyngeal perforations.139 Others who have evaluated this form of treatment with thoracic esophageal perforations have selected larger perforations for surgical treatment.133 There is also a chance of reporting bias where failures of conservative approach may not be reported. In addition, as emphasized by Pasricha et al., it is quite difficult to predict that a small perforation selected for conservative management will not progress to cause extensive mediastinitis.138 Thus, early surgery should still be considered the treatment of choice for most patients, with conservative treatment reserved for selected cases (Table 16.10).

257

Table 16.10 Selection guidelines for nonoperative management of esophageal perforation Minimal pain Absence of shock Mild to moderate fever or leukocytosis No clinical evidence of sepsis A confined cavity that drains well into the esophagus Delayed diagnosis >24 hours, no progression or patient improving Adapted from Pasricha et al.119

SUMMARY Nearly 100 drugs have been reported to cause injury to the esophageal mucosa. Such injury may be an acute, superficial injury that heals rapidly or deep, intramural ulceration, which heals by stricture formation. Esophageal injury caused by medications is entirely preventable. A periodic, careful history for odynophagia, retrosternal pain, and dysphagia should be obtained. Concomitant therapy with anticholinergics should be avoided, and liquid preparations should be used for bed-confined patients or those with esophageal strictures, diverticula, or dysmotility. Early barium swallow

or endoscopy is indicated, and symptomatic treatment using antacids, topical xylocaine gel, or both are useful. Drug-induced deep esophageal ulcers are slow to heal and acid suppression is indicated. Tight, fibrotic strictures may require diligent, multiple fluoroscopic and wire-guided dilations, while intralesional corticosteroid injections and surgery have no proven role. Esophageal damage caused by chemotherapy and chemoradiation therapy is often diffuse and involves long segments. Pain control followed by healing is the goal of therapy; viscous lidocaine, systemic analgesics, sucralfate, and PPIs appear to provide benefit. Lye-based liquid household cleaners along with foreign body aspiration are the third most common cause of pediatric death in the United States. Industry-wide voluntary and legislative efforts are needed for effective prevention. These patients typically present with nausea, vomiting, dysphagia, refusal to drink, drooling, and stridor. In the first 72 hours after ingestion, airway protection is the primary goal. Management in the intensive care unit with intravenous fluids, pressors, and antibiotics is useful. Early surgical consultation is needed when viscous perforation is suspected. In the absence of perforation, early endoscopy with a small, flexible endoscope is safe and necessary for assessment of severity. Acute corrosive injury may be managed conservatively with broadspectrum antibiotics, thin-caliber nasogastric suction tube placement, and intensive care management with arguable success. Esophageal dilation carried out in the subacute phase (3 days to 3 weeks) is risky but may be successful. Frequent, painfully diligent sessions over several months may be needed.

Summary

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Fig. 16.8 A radiograph of the neck showing diffuse subcutaneous emphysema.The patient had a microperforation following esophageal dilation for Zenker diverticulum and prominent cricopharyngeal bar.

Treatment of Esophageal Disorders caused by Medications, Caustic Ingestion, Foreign Bodies and Trauma

258 Due to their potential for causing rapid damage, button batteries must be kept out of the reach of children. Prompt identification and location of the battery by radiography is the most important first step. If the battery is lodged in the esophagus, a prompt endoscopic extraction is mandatory, using a basket or a net device as the method of choice. Airway protection by endotracheal intubation and the use of an overtube are critical. Neutralizing agents and emetic agents are generally ineffective. Early surgery may be indicated if a perforation, full-thickness injury, or fistula formation is detected by endoscopy. Similarly, other foreign bodies or food bolus require emergent removal in the presence of respiratory distress, location of the foreign body at the cricopharyngeus level, inability to swallow secretions, sharp object ingestion, or evidence of perforation. With increasing availability of diagnostic and therapeutic endoscopy, iatrogenic trauma to the esophagus has become more common. Endoscopic ablation of esophageal lesions by thermoablative techniques, photodynamic therapy, and radiofrequency devices has added a new dimension to the iatrogenic esophageal injury. Nevertheless, management principles remain the same, with prompt identification of the injury being the key. Although the use of conservative management is being reported, surgical repair remains the mainstay of management when perforation is strongly suspected.

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